The heart includes a number of pathways through which electrical signals necessary for normal, electrical and mechanical synchronous function of the upper and lower heart chambers propagate. Tachycardia, that is abnormally rapid rhythms of the heart, is caused by the presence of an arrhythmogenic site or accessory pathway, which bypasses or short circuits the nodal pathways in the heart. Tachycardias may be categorized as ventricular tachycardias (VTs) or supraventricular tachycardias (SVTs). The most common SVTs include atrioventricular nodal reentrant tachycardia (AVNRT), Atrioventricular reentrant tachycardia (AVRT), atrial fibrillation (AF), and atrial flutter (AFI). Reentrant tachycardias originate in the atria and are typically caused by an accessory pathway or inappropriate premature return excitation from the ventricle through the AV node or left sided accessory pathway. Conditions such as AF and AFI involve either premature excitation from focal ectopic sites within the atria or excitations coming through inter-atrial reentry pathways as well as regions of slow conduction within the atria. VTs originate from within the ventricles and have their entire circuit contained within the ventricles. These VTs include bundle branch reentrant tachycardia (BBR), right ventricular outflow tract tachycardia (RVOT), and ventricular fibrillation (VF). VTs are often caused by arrhythmogenic sites associated with a prior myocardial infarction as well as reentrant pathways between the ventricles. BBR involves an inappropriate conduction circuit that uses the right and left bundle branches. RVOT can be described as a tachycardia originating from the right ventricular outflow tract, which involves ectopic triggering or reentry mechanisms. VF is a life threatening condition where the ventricles entertain a continuous uncoordinated series of contractions that cause a cessation of blood flow from the heart. If normal sinus rhythm is not restored, the condition is terminal.
Treatment of both SVTs and VTs may be accomplished by a variety of approaches, including drugs, surgery, implantable electrical stimulators, and catheter ablation of cardiac tissue of an effected pathway. While drugs may be the treatment of choice for many patients, drugs typically only mask the symptoms and do not cure the underlying cause. Implantable electrical stimulators, e.g., pacemakers, afferent nerve stimulators and cardioverter/defibrillators, which have proven to provide successful treatment, usually can only correct an arrhythmia after it occurs and is successfully detected. Surgical and catheter-based treatments, in contrast, will actually cure the problem usually by ablating the abnormal arrhythmogenic tissue or accessory pathway responsible for the tachycardia. The catheter-based treatments rely on the application of various destructive energy sources to the target tissue including direct current electrical energy, radio frequency (RF) electrical energy, laser energy, ultrasound, microwaves, and the like.
RF ablation protocols have proven to be highly effective in treatment of many cardiac arrhythmias while exposing the patient to minimum side effects and risks. RF catheter ablation is generally performed after an initial electrophysiologic (EP) mapping procedure is conducted using an EP mapping catheter to locate the arrhythmogenic sites and accessory pathways. After EP mapping is completed, an RF ablation catheter having a suitable electrode is introduced to the appropriate heart chamber and manipulated so that the electrode lies proximate the target tissue. Such catheters designed for mapping and ablation, frequently include one or more cylindrical or band-shaped individual electrodes mounted to the distal section of the catheter so as to facilitate mapping of a wider area in less time, or to improve access to target sites for ablation. RF energy is then applied through the electrode(s) to the cardiac tissue to ablate a region of the tissue that forms part of the arrhythmogenic site or the accessory pathway.
Such mapping and ablation catheters are inserted into a major vein or artery, usually in the neck or groin area, and guided into the chambers of the heart by appropriate manipulation through a venous or arterial route, respectively. The catheter must have a great deal of flexibility or steerability to be advanced through the vascular system into a chamber of the heart, and the catheter must permit user manipulation of the tip even when the catheter body traverses a curved and twisted vascular access pathway. Such catheters must facilitate manipulation of the distal tip so that the distal electrode(s) can be positioned and held against the tissue region to be mapped or ablated.
The arrhythmogenic sites or accessory pathways to be mapped and ablated frequently occur within the left atrial wall, particularly around pulmonary vein orifices. It is preferable in such cases to introduce an instrument into the right atrium by a venous route including the inferior vena cava and to advance it through the septum separating the right and left atrium. In one exemplary approach, a guide catheter is inserted in this manner into the right atrium, and instruments are introduced through the guide catheter lumen that are manipulated from their proximal end and advanced through the septal wall first creating a very small trans-septal perforation, and then enlarging the perforation by dilation or the like. The guide catheter is then advanced over the instruments or advanced directly through the perforation in the septal wall to locate the guide catheter distal end within the left atrial chamber. The penetrating instruments are retracted from the guide catheter lumen. The proximal end of the guide catheter is typically taped to the patient's body or a support to inhibit retraction back into the right atrial chamber. The mapping and ablation catheters are then inserted through the guide catheter lumen to locate their distal segments within the left atrial chamber.
The mapping and ablation procedures are undertaken, the mapping and ablation catheters are retracted, and the guide catheter is also retracted. The trans-septal perforation tends to shrink as the dilated myocardial tissue expands across the perforation.
It is important that the distal segment of the guide catheter inserted through the septum remain in place for the entire procedure and not slip back into the right atrium. The guide catheter can be inadvertently dislodged by movements of the proximal segment emerging from the site of incision. The dislodgement can require withdrawal of the instruments in use, jeopardizing their sterility, while delay occurs in reestablishing catheter position and resumption of the procedure.
In addition, the only way to monitor the location of the distal segment of the guide catheter is through visualization of a radiopaque marker of the guide catheter in regard to recognizable physiologic features of the heart.
It is sometimes necessary that the distal end segment of the electrophysiology catheter be directed at an acute angle just as it exits the guide catheter lumen to be directed toward certain features of the left atrium. Therefore, only a very short distal segment of the guide catheter is extended into the left atrium past the septum so that the electrophysiology catheter can be directed to the feature of interest. It is more difficult to maintain the distal segment within the left atrium as the distal segment within the left atrium is shortened.
There is therefore a need for a guide catheter that does not readily retract through the septum once it has been extended through the septum.